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156<br />
117 <br />
P<br />
ABCG <br />
1 2 1 1<br />
1<br />
2 <br />
<br />
5aminolevulinic acid ALA PDD <br />
PDT <br />
ALA protoporphyrin IX PpIX <br />
imatinib ATPbinding cassette ABC<br />
transporter G2 ABCG2 PpIX <br />
genistein ALA PpIX<br />
PDD PDT <br />
genistein ALA PpIX <br />
ABCG2 <br />
ABCG2 Ko143 <br />
genistein doxorubicin <br />
genistein <br />
PpIX <br />
PpIX ALAgenistein incubation <br />
<br />
genistein ALA PDD PDT <br />
<br />
P<br />
<br />
P<br />
DGKε <br />
<br />
<br />
DGK<br />
C DG <br />
DGKDGKε<br />
DGK / DG<br />
<br />
DGKε <br />
DGKε <br />
DGKε <br />
N DGKεNhalf <br />
DGKεKD <br />
DGKε ER tracker calreticulin <br />
DGKε <br />
DGKεNhalf<br />
DGKεKD <br />
DGKε N <br />
<br />
P<br />
DGKζ NAP DGKζ <br />
<br />
<br />
DGK C <br />
<br />
HeLa DNA <br />
Doxorubicin p53 <br />
DGKζ <br />
p53 <br />
<br />
MG132 p53 <br />
<br />
<br />
DGKζ Nucleosome<br />
assembly protein NAP 1 NAP2 DGKζ <br />
HeLa DNA p53 <br />
DGKζ <br />
NAP1/NAP2 p53 <br />
NAP DGKζ p53 <br />
<br />
P<br />
Cellular localization of ERα and their apoptotic effects<br />
<br />
<br />
The actions of estrogen have traditionally been thought to occur through binding<br />
estrogen receptors in nucleus. Recent data, however, support the idea that some<br />
of ERα in the cytoplasm of various target cells are localized in mitochondria.<br />
Moreover, ERα collaborates with a number of factors on cell membrane, in<br />
cytoplasm, and nucleus to effectively modulate transcription of distinctive<br />
groups of target genes. While some of these factors appear to regulate the<br />
chromatin configuration by controlling histone modifications at the promoter,<br />
others are members of various kinase cascades. In order to discern functions and<br />
interactions of ERα and its coregulators, we allocated ERα to different locations<br />
in ERαnegative Ishikawa cell, using permanent transfection technique. In this<br />
report the antiapoptotic effects were examined for ERα at different cellular<br />
locations in the presence of inhibitors for EGFR, PI3K, MEK, and p38MAPK.<br />
Cellular alterations in proliferation, membrane potential, and caspase activities<br />
were examined using immunohistochemistry, flow cytometry, and related<br />
techniques. The present results might shed light on different pathways of ERα<br />
signal transduction.<br />
P<br />
<br />
<br />
1,2 1 1 1,2 3 <br />
2 1<br />
1<br />
2 2 2 <br />
3<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
<br />
PERKeIF2α Western blotting <br />
WST1 assay <br />
DNA ladder <br />
eIF2α <br />
eIF2α CHOP <br />
<br />
3% <br />
DNA